Sleep apnea is a serious malady ranking second only to insomnia as the most prevalent sleep disorder. Symptoms of sleep apnea include snoring, breath holding during sleep, rapid awakening with gasping for air, morning headaches, depression, irritability, loss of memory, lack of energy, and high risk of automobile and workplace accidents.
Apnea occurs when breathing difficulty causes the oxygenation of blood and body tissues to fall dangerously low. The brain often reacts by directing a release of adrenalin, which can arouse the apneic patient. Thereafter, regular breathing and normal exchange of oxygen and accumulated carbon dioxide resumes. Severe sleep apnea, however, may result in hundreds of episodes of oxygen desaturation during 6–8 hours of attempted sleep. The typical sleep apnea patient is not conscious of the struggle for oxygen, but may feel tired and ill in the morning.
Sleep apnea has multiple classifications based on the source of dysfunction. Obstructive sleep apnea results from mechanical blockage of the airway, for example, due to the weight of fatty neck tissue compressing the trachea. Central sleep apnea results from neurological dysfunction. Mixed sleep apnea has a combination of mechanical and neurological cause.
Sleep apnea can be life-threatening, especially when it occurs in conjunction with coronary artery disease (CAD) or congestive heart failure (CHF or “heart failure”). Not only does sleep apnea place a tremendous burden on the heart and the entire cardiopulmonary system directly, but it also circumvents the normal architecture of human sleep, which affects the heart indirectly. The apnea-induced alteration of the sleep cycle, including reduced slow-wave (deep) and REM (dream) segments, causes sleep to be ineffective. A vicious cycle follows as an unremitting sleep debt and daytime weariness worsen CAD, CHF, and hypertension. Consequently, sleep apneics who have a blood oxygen level lowered by sleep-disordered breathing are at an increased risk for hypertension, arrhythmias, heart attack, stroke, and nocturnal sudden death.
Approximately fifty percent of patients with heart failure suffer from sleep apnea. About ten percent of the heart failure patients suffer from obstructive sleep apnea, while about forty percent of patients with heart failure suffer from central sleep apnea. A high comorbidity exists between sleep apnea and certain types of CHF, which results from a negative synergy between the gas exchange problem due to mechanical breathing dysfunction during apnea and the oxygen distribution problem caused by weak pumping and fluid buildup characteristic of CHF. CHF is a condition in which a weakened heart cannot pump enough blood to body organs. Failing myocardium due to CHF may affect either the pumping action of the right side, left side, or both sides of the heart. The weak pumping action causes fluid to back up into other areas of the body including the liver, gastrointestinal tract, and extremities (right-sided heart failure), or the lungs (left-sided heart failure). Heart failure patients have characteristic pulmonary edema or pitting edema of the lower legs.
Sleep apnea may be treated by administering continuous positive airway pressure (CPAP) via a machine or by various other treatments, such as surgery and medications. The type of treatment depends on the type of sleep apnea. It is generally believed that reducing heart failure symptoms reduces the apnea burden, which in turn further reduces the heart failure symptoms. Cardiac pacing can also affect sleep apnea. There is a need to improve the techniques for applying pacing therapy from implantable cardiac devices in a manner that effectively combats sleep apnea.